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经皮穿刺引流术是治疗化脓性肝脓肿的基石。

Hypercapsule is the cornerstone of in inducing pyogenic liver abscess.

机构信息

Department of Laboratory Medicine, Huashan Hospital, Fudan University, Shanghai, China.

Department of Infectious Diseases, Huashan Hospital, Fudan University, Shanghai, China.

出版信息

Front Cell Infect Microbiol. 2023 Mar 31;13:1147855. doi: 10.3389/fcimb.2023.1147855. eCollection 2023.

DOI:10.3389/fcimb.2023.1147855
PMID:37065211
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10102340/
Abstract

PURPOSE

To investigate the mechanisms of -induced pyogenic liver abscess (PLA).

METHODS

Forty-three strains from PLAs and 436 from non-PLAs were collected. Their differences were compared for virulence genes and factors, sequence types, and serotypes. Virulence genes , , and + were deleted in NTUH-K2044. Various analyses, such as transmission electron microscopy, neutrophil killing tests, and mouse lethality tests, were used to confirm the consequent changes.

RESULTS

Differences were found between strains from PLA and non-PLA samples for virulence genes and factors, including metabolism genes ( and ), capsular polysaccharide (CPS)-synthesis channel gene (), CPS-regulating genes (, , and ), and siderophore genes ( and ). When was positive, the difference between PLA and non-PLA samples was only observed with . Δ, Δ, and ΔΔ strains reverted to hypovirulence. In the Kupffer cell stimulation assay, interleukin (IL)-6, IL-12, IL-10, and transforming growth factor-β secretions were found to be equivalent in NTUH-K2044, Δ, Δ, and ΔΔ groups. Lower IL-1β and higher tumor necrosis factor-α secretions were observed for Δ, Δ, and ΔΔ.

CONCLUSIONS

Hypercapsule production is the cornerstone of hypervirulence, regardless of exopolysaccharides. K1 -induced PLA may decrease core inflammatory cytokines rather than increase anti-inflammatory cytokines. Exopolysaccharides could also attenuate the inflammatory response to aid in the immune escape of .

摘要

目的

研究 - 诱导的化脓性肝脓肿(PLA)的机制。

方法

收集 43 株 PLA 株和 436 株非 PLA 株。比较它们的毒力基因和因子、序列型和血清型差异。在 NTUH-K2044 中缺失了毒力基因 、 、 和 +。使用透射电子显微镜、中性粒细胞杀伤试验和小鼠致死性试验等各种分析方法来确认随后的变化。

结果

PLA 和非 PLA 样本的 株之间在毒力基因和因子方面存在差异,包括代谢基因( 和 )、荚膜多糖(CPS)合成通道基因()、CPS 调节基因( 、 、和 )和铁载体基因( 和 )。当 为阳性时,仅在 PLA 和非 PLA 样本之间观察到 。Δ 、Δ 和 ΔΔ 菌株的毒力减弱。在 Kupffer 细胞刺激试验中,发现 NTUH-K2044、Δ 、Δ 和 ΔΔ 组的白细胞介素(IL)-6、IL-12、IL-10 和转化生长因子-β分泌相当。Δ 、Δ 和 ΔΔ 组的 IL-1β 分泌较低,肿瘤坏死因子-α 分泌较高。

结论

高荚膜产生是高毒力的基石,与外多糖无关。K1 诱导的 PLA 可能会降低核心炎症细胞因子,而不是增加抗炎细胞因子。外多糖也可以减轻炎症反应,帮助 逃避免疫。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11b4/10102340/5a14611b6cf7/fcimb-13-1147855-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11b4/10102340/950e025df876/fcimb-13-1147855-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11b4/10102340/1382a2f4ee64/fcimb-13-1147855-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11b4/10102340/dc1f05d0076e/fcimb-13-1147855-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11b4/10102340/5a14611b6cf7/fcimb-13-1147855-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11b4/10102340/950e025df876/fcimb-13-1147855-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11b4/10102340/1382a2f4ee64/fcimb-13-1147855-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11b4/10102340/dc1f05d0076e/fcimb-13-1147855-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11b4/10102340/5a14611b6cf7/fcimb-13-1147855-g004.jpg

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